The mechanisms responsible for the production of experimental allergic encephalomyelitis, a model of autoimmune disease are being examined. Current research is focused on an adoptively transferred model which is produced by the transfer of lymphocytes sensitized against myelin basic protein in syngeneic animals. Under optimal conditions, neurological dysfunction occurs; this is characterized pathologically by inflammation and primary demyelination. Many mice recover and develop chronic-relapsing disease. The mechanisms responsible for both the initial and the chronic disease are not known, but an early event is the migration of immune cells across the blood-brain barrier into the central nervous system. This is formed by the capillary endothelial cells. Other cells in close proximity are astrocytes and microglia. Antigen presentation by macrophages, capillary endothelial cells in the brain, and astrocytes are being compared. The expression of MHC molecules on these cells is also being evaluated. An encephalitogenic epitope for SJL mice has been identified and T-cell lines against this have been derived. These both proliferate and show cytotoxic activity.